The skin covers the surface of the body and consists of two main layers, the epidermis and the subjacent connective tissue layer -- the corium, or dermis. The epidermis is a stratified squamous epithelium, the external layer of which keratinizes, or cornifies. The hairs are slender keratinous threads which develop from the matrix cells of the follicular epithelium. Each hair arises in a tubular invagination of the epidermis, the hair follicle, the walls of which are composed of epithelial and connective tissue. One or more sebaceous glands are connected with each hair. Through a short duct they empty their excretion product into the follicular canal in the upper third of its length. In sebaceous glands the secretions result from the destruction of the epithelial cells. These cells break down yielding the oily secretion of the gland, and also a small number of cornified cells.
The epithelial layers are subject to constant mechanical and other trauma. Under certain physiological conditions their cells perish continuously and are shed. This is especially manifest in the epidermis, where the superficial cells are continuously undergoing a peculiar degeneration, called cornification. The cornified cells are constantly desquamated and are replaced by new ones which arise through transformation of the cells of the deeper layers. Part of this transformation involves the oxidation of protein sulfhydryl groups found in keratin (RSH) to disulfides (R--S--S--R). Thus, the surface of the skin contains a large percentage of the protein keratin which is characterized by many disulfide bonds. Under certain circumstances, excessive cornification occurs, and a condition known as hyperkeratinization (hyperkeratosis) develops. (The Cyclopedia of Medicine, Surgery and Specialities, G. M. Piersol, Ed., F. A. Davis Co., Philadelphia, 1946, P. 107.)
The pathological changes common to acne vulgaris consist of a follicular hyperkeratosis and a hypersecretion of sebum. The result of this process is the comedo, or "blackhead," which is composed at its outer end of concentric layers of horny cells, dried sebum, acne bacillus and staphylococci, and at its inner end mainly of sebum. The outer end of the comedo is dark-colored from oxidation of the sebum as well as from dirt. The pressure of the comedo causes some atrophy of the epithelium of the follicle. Sometimes the hyperkeratosis of the mouths of the follicles closes them completely, so that small sebaceous cysts are formed rather than comedones.
Waiting for the spontaneous cure of acne may have tragic results. Early treatment may prevent the number of scars and pits. Many therapeutic procedures have been used. However, the number of new preparations constantly appearing indicates that none of the procedures now used are entirely satisfactory. These methods of treatment include the following: (1) Diet; (2) Keratolytic agents; (3) Antibiotics; (4) Estrogens; (5) Vitamin A; (6) Ultraviolet radiation; (7) Roentgen ray therapy; (8) Surgical removal; and other less frequently used measures. Some of these methods are aimed at decreasing sebaceous gland secretions, others at removing some of the cornified layer of skin or at reducing infection or inflammation. Each of these has undesirable features, however, even though they may produce an amelioration of the acne.
Thioglycolic acid has been used in hair waving lotions and depilatory creams. Other thiol compounds, for example, 2-mercaptopyridine-N-oxide, have been used in shampoos for their antiseptic properties. Topical ointments available for the treatment of diaper rash have been known to contain cysteine. However, the utility of thioglycolic acid and its salts for the treatment of acne and similar dermatological disorders has not been observed previously.